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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analysis of the Framingham data has shown that the risk of heart failure is increased substantially among diabetic patients, while persons with the metabolic syndrome have an increased risk of both atherosclerosis and diabetes mellitus. Sleep apnea may be related to the metabolic syndrome and systemic inflammation through hypoxia, which might also cause the cardiac remodeling by increased oxidative stress. On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor. Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes. Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.
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PMID:Regulation of oxidative stress and cardioprotection in diabetes mellitus. 2006 32

Chronic kidney disease (CKD) is characterized by irreversible pathological processes that result in the development of end-stage renal disease (ESRD). Accumulating evidence has emphasized the important role of chronic hypoxia in the tubulointerstitium in the final common pathway that leads to development of ESRD. The causes of chronic hypoxia in the tubulointerstitium are multifactorial and include mechanisms such as hemodynamic changes and disturbed oxygen metabolism of resident kidney cells. Epidemiological studies have revealed an association between CKD and systemically hypoxic conditions, such as chronic obstructive pulmonary disease and sleep apnea syndrome. In addition to tubulointerstitial hypoxia, glomerular hypoxia can occur and is a crucial factor in the development of glomerular disorders. Chemical compounds, polarographic sensors, and radiographical methods can be used to detect hypoxia. Therapeutic approaches that target chronic hypoxia in the kidney should be effective against a broad range of kidney diseases. Amelioration of hypoxia is one mechanism of inhibiting the renin-angiotensin system, the current gold standard of CKD therapy. Future therapeutic approaches include protection of the vascular endothelium and appropriate activation of hypoxia-inducible factor, a key transcription factor involved in adaptive responses against hypoxia.
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PMID:The suffocating kidney: tubulointerstitial hypoxia in end-stage renal disease. 2087 4

This review considers the 250+ papers concerning the association of the angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism (rs1799752) and various disease conditions published in 2009. The deletion allele occurs in approximately 55% of the population and is associated with increased activity of the ACE enzyme. It might be predicted that the D allele, therefore, might be associated with pathologies involving increased activity of the renin-angiotensin system. The D allele was seen to be associated with an increased risk of hypertension, pre-eclampsia, heart failure, cerebral infarct, diabetic nephropathy, encephalopathy, asthma, severe hypoglycaemia in diabetes, gastric cancer (in Caucasians) and poor prognosis following kidney transplant. On the positive side, the D allele appears to offer protection against schizophrenia and chronic periodontitis and confers greater up-per-body strength in old age. The I allele, meanwhile, offers improved endurance/athletic performance and aerobic capacity as determined by lung function tests, although it does increase the risk of oral squamous cell carcinoma and obstructive sleep apnoea in hypertensives.
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PMID:Implications of the angiotensin converting enzyme gene insertion/deletion polymorphism in health and disease: a snapshot review. 2153 87

Corticosteroids constitute an ideal treatment for various inflammatory and autoimmune disorders due to their anti-inflammatory and immunomodulatory actions. However, corticosteroids have a considerable number of side effects, including hypertension, diabetes, lipid disorders, sleep apnea, osteoporosis, myopathy, and disorders of coagulation and fibrinolysis, which are components of Cushing's syndrome (CS). Corticosteroid-induced side effects are dependent on the formulation, route, dose, and time of exposure. However, the underlying pathogenetic mechanisms have not been clearly defined. A large body of evidence supports the role of an imbalance between vasoconstriction and vasodilation with possible links to nitric oxide, prostanoids, angiotensin II, arginine vasopressin, endothelins, catecholamines, neuropeptide Y, and atrial natriuretic peptide. Increased oxidative stress, renin-angiotensin system activation, increased pressor response, metabolic syndrome, and sleep apnea appear to be pathogenetically involved as well. The ideal treatment is the withdrawal of corticosteroids, which is most often impossible due to the exacerbation of the underlying disease. Alternatively, a careful plan, including the proper selection of the formulation, time, and route, should be made, and each side effect should be treated properly. The focus of the research should be to develop synthetic corticosteroids with anti-inflammatory effects but fewer metabolic effects, which so far has been unsuccessful.
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PMID:Hypertension and other morbidities with Cushing's syndrome associated with corticosteroids: a review. 2194 34

We will review some diseases that interfere most with management of heart failure : anemia, chronic renal failure, chronic pulmonary diseases, diabetes, atrial fibrillation/flutter, sleep apnea, angina, systemic arterial hypertension, rheumatic disease, depression and anticancer chemotherapy. We will retain principally their therapeutic implications. Anemia can be partially corrected by administration of intravenous iron or erythropoietin. Chronic renal failure requires adaptation of the treatment, in particular for drugs of the renin-angiotensin-aldosterone system. Chronic pulmonary diseases complicate diagnosis of heart failure and may lead to sub prescription of beta-blockers. Diabetes does not alter the usual recommendations for the treatment of heart failure but some hypoglycemic medications should be prescribed with caution. In the presence of atrial fibrillation or flutter, the main purpose of the treatment is to improve the quality of live and to diminish the thromboembolic risk ; it may be obtained by rhythm or rate control. Therapeutic approach of sleep apnea is based on optimal treatment of heart failure and weight loss. In the presence of angina, systemic arterial hypertension, rheumatic disease or depression, certain drugs usually prescribed are contraindicated or must be prescribed with caution. Finally, chemotherapy can be cardiotoxic and require careful monitoring of cardiac function.
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PMID:[Management of comorbidities in heart failure]. 2395 55

Peripheral chemoreceptors in the carotid body play important roles in the transduction of chemical stimuli in the arterial blood to the central for eliciting the chemoreflex, which mediates the ventilatory and circulatory responses to hypoxia. The activity of carotid chemoreceptor is modulated and significantly contributes to the ventilatory acclimatization at high altitude. In addition, the carotid chemoreceptor activity is augmented in patients with sleep-disordered breathing, notably in central or obstructive sleep apnea, and also in experimental animals. Thus, the carotid body functions to maintain the oxygen homeostasis, whereas anomalous carotid chemoreceptor activities could be both adaptive and pathogenic in sleep apnea. This review aims to summarize the cellular and molecular mechanisms that could mediate the augmented chemoreceptor activity induced by intermittent hypoxia. Our recent findings suggest a pathogenic role of inflammation mediated by an upregulation of renin-angiotensin system in the carotid body in the over-activity of the chemoreflex. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body function, which could play a role in the pathophysiology of sleep apnea.
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PMID:Mechanisms of maladaptive responses of peripheral chemoreceptors to intermittent hypoxia in sleep-disordered breathing. 2455 66

Obstructive sleep apnea (OSA) is an independent risk factor for hypertension and cardiovascular disease. OSA is the frequent underlying disease of secondary hypertension and resistant hypertension. In 2003, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure recognized sleep apnea as a common and identifiable cause of hypertension and suggested blood pressure screening among patients with OSA. OSA increases both daytime and nocturnal ambulatory blood pressures through the activation of various neurohumoral factors including the sympathetic nervous system and the renin-angiotensin-aldosterone system. Randomized, controlled trials have evaluated the use of continuous positive airway pressure (CPAP) to reduce BP among persons with OSA. The benefits of OSA treatment are related to implications for hypertension management.
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PMID:[Sleep apnea syndrome: SAS]. 2516 50

The renin-angiotensin system (RAS) plays pivotal roles in the regulation of cardiovascular and renal functions to maintain the fluid and electrolyte homeostasis. Experimental studies have demonstrated a locally expressed RAS in the carotid body, which is functional significant in the effect of angiotensin peptides on the regulation of the activity of peripheral chemoreceptors and the chemoreflex. The physiological and pathophysiological implications of the RAS in the carotid body have been proposed upon recent studies showing a significant upregulation of the RAS expression under hypoxic conditions relevant to altitude acclimation and sleep apnea and also in animal model of heart failure. Specifically, the increased expression of angiotensinogen, angiotensin-converting enzyme and angiotensin AT1 receptors plays significant roles in the augmented carotid chemoreceptor activity and inflammation of the carotid body. This review aims to summarize these results with highlights on the pathophysiological function of the RAS under hypoxic conditions. It is concluded that the maladaptive changes of the RAS in the carotid body plays a pathogenic role in sleep apnea and heart failure, which could potentially be a therapeutic target for the treatment of the pathophysiological consequence of sleep apnea.
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PMID:The role of local renin-angiotensin system in arterial chemoreceptors in sleep-breathing disorders. 2524 81

The prevalence of chronic kidney disease (CKD) is increasing, which presents challenges for both patients and health-care budgets. Although this phenomenon has been attributed to the growth in diabetes, hypertension, and obesity, sleep apnea and nocturnal hypoxemia may also contribute to the pathogenesis of CKD and its progression to kidney failure. Two pathophysiologic mechanisms responsible for CKD are glomerular hyperfiltration and chronic intrarenal hypoxia, resulting in tubulointerstitial injury, the final common pathway to end-stage kidney disease (ESKD). Multiple descriptive studies have demonstrated an association between CKD and sleep apnea. Although sleep apnea is common in patients with CKD and associated with significant nocturnal hypoxemia, it is often relatively free of sleep-related symptoms, making it difficult to detect without objective nocturnal monitoring. Nevertheless, sleep apnea and nocturnal hypoxemia have been associated with loss of kidney function and kidney injury, suggesting that they contribute to the pathogenesis of continued deterioration in kidney function. There are several pathways through which sleep apnea may achieve this, including a direct effect of intrarenal hypoxia and activation of the systemic and renal renin-angiotensin system. Further research is required to better understand these relationships and determine whether specific interventions in patients with sleep apnea have an impact on clinical outcomes, such as reducing the prevalence of CKD and delaying its progression to ESKD.
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PMID:Sleep apnea and the kidney: is sleep apnea a risk factor for chronic kidney disease? 2528 1

A small proportion of the treated hypertensive population consistently has a blood pressure greater than 140/90 mm Hg despite a triple therapy including a diuretic, a calcium channel blocker, and a blocker of the renin-angiotensin system. According to guidelines, these patients have so-called resistant hypertension. The prevalence of this clinical condition is higher in tertiary than primary care centers and often is associated with chronic kidney disease, diabetes, obesity, and sleep apnea syndrome. Exclusion of pseudoresistant hypertension using ambulatory or home blood pressure monitoring is a crucial step in the investigation of patients with resistant hypertension. Thus, among the multiple factors to consider when investigating patients with resistant hypertension, ambulatory blood pressure monitoring should be performed very early. Among other factors to consider, physicians should investigate patient adherence to therapy, assess the adequacy of treatment, exclude interfering factors, and, finally, look for secondary forms of hypertension. Poor adherence to therapy accounts for 30% to 50% of cases of resistance to therapy depending on the methodology used to diagnose adherence problems. This review discusses the clinical factors implicated in the pathogenesis of resistant hypertension with a particular emphasis on pseudoresistance, drug adherence, and the use of ambulatory blood pressure monitoring for the diagnosis and management of resistant hypertension.
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PMID:Ambulatory blood pressure and adherence monitoring: diagnosing pseudoresistant hypertension. 2541 58


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